Infarto agudo del miocardio como primera manifestación del síndrome antifosfolípido primario en un paciente de veinticuatro años

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Abstract

El síndrome antifosfolípido primario usualmente se manifiesta como trombosis venosa profunda, tromboembolismo pulmonar y como evento cerebrovascular en la circulación arterial. Se presenta el caso de un paciente joven previamente sano, con infarto agudo del miocardio como primera manifestación del síndrome antifosfolípido primario.

Translated abstract

Primary antiphospholipid syndrome is usually manifested with deep venous thrombosis, pulmonary thromboembolism and arterial thrombosis, including cerebrovascular accidents. We report the case of a previously healthy young patient who suffered an acute myocardial infarction as the first manifestation of a primary antiphospholipid syndrome.

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The lupus anticoagulant is a risk factor for myocardial infarction (but not atherosclerosis): Hopkins Lupus Cohort.

Michelle Petri (2003)

Antiphospholipid antibodies, both anticardiolipin and lupus anticoagulant, are common in SLE. We asked, in a prospective cohort, whether these antibodies are predictive of atherosclerosis and/or coronary artery disease. Three hundred eighty patients, 92% female, 49% Caucasian, 51% African-American, mean age 46.4+/-12.3 years are followed quarterly, with assessment of both anticardiolipin and lupus anticoagulant (dRVVT). These patients underwent both helical CT and carotid duplex. Both the lupus anticoagulant and anticardiolipin are predictive of later venous or arterial thrombosis. Twenty years after diagnosis, SLE patients with the lupus anticoagulant (LA) have a 50% chance of a venous thrombotic event. Myocardial infarction occurs significantly more often in those with LA 22% vs. 9%, p=0.04. Neither anticardiolipin nor LA are associated with carotid IMT, carotid plaque, nor coronary calcium by helical CT. In aCL positive patients carotid IMT was 0.57+/-0.01 vs. 0.58+/-0.01 in aCL negative patients (p=NS); carotid plaque 0.47+/-0.13 vs. 0.32+/-0.10 (p=NS); and coronary calcium 65.4+/-37.4 vs. 65.4+/-30.2 (p=NS). In LA positive patients, carotid IMT was 0.59+/-0.03 vs. 0.59+/-0.02 in LA negative patients (p=NS); carotid plaque 0.07+/-0.02 (SE) vs. 0.80+/-0.02 (SE) (p=0.06); and coronary calcium 28.1+/-3.7 (SE) vs. 85.7+/-2.6 (SE) (p=NS). Antiphospholipid antibodies are not associated with subclinical atherosclerosis (carotid IMR, carotid plaque, helical CT coronary calcium), but are associated with actual thrombotic sequelae (myocardial infarction).

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Myocardial infarction caused by cardiac microvasculopathy in a patient with the primary antiphospholipid syndrome.

J Klenz, S. Labib, H Aretz … (1992)

Antiphospholipid antibodies occur in various clinical states, including the primary antiphospholipid syndrome. Clinical features in these conditions appear to be caused by vasculopathy associated with the presence of these antibodies. We report the case of a patient with primary antiphospholipid syndrome who experienced cardiac necrosis secondary to myocardial microvasculopathy in the absence of vasculitis. This case demonstrates unequivocally that noninflammatory myocardial microvasculopathy occurs in the primary antiphospholipid syndrome per se without any clinical or immunologic signs of systemic lupus erythematosus or other disease process. The histopathologic findings in the skin and myocardial biopsies showed a noninflammatory vasculopathy characterized by bland thrombi and lack of infiltration of the vessel wall by inflammatory cells. Ultrastructural examination of the myocardial biopsy confirmed the vascular thrombosis and endothelial activation and showed no deposits in basement membranes. The patient survived after appropriate treatment. Evidence presented here supports the concept that the vasculopathy in the antiphospholipid syndrome is distinct from other types of vascular occlusions seen in systemic lupus erythematosus. We suggest that myocardial biopsy can be crucial in showing an underlying myocardial ischemic process despite "normal" findings on coronary angiography. Results of the biopsy hastened the decision to use potentially lifesaving plasmapheresis and anticoagulation therapy in this patient.